Outdoor air pollution and respiratory health in patients with COPD - Thorax

[Pages:6]Chronic obstructive pulmonary disease

Thorax: first published as 10.1136/thx.2010.155358 on 1 April 2011. Downloaded from on January 11, 2024 by guest. Protected by copyright.

Outdoor air pollution and respiratory health in patients with COPD

Janet L Peacock,1 H Ross Anderson,2 Stephen A Bremner,3 Louise Marston,4 Terence A Seemungal,5 David P Strachan,2 Jadwiga A Wedzicha5

< Additional tables and methods are published online only. To view these files please visit the journal online (http:// thorax.).

1Department of Primary Care and Public Health Sciences, King's College London, London, UK 2Department of Community Health Sciences, St George's, University of London, London, UK 3Queen Mary University of London, Barts and the London School of Medicine and Dentistry, Centre for Health Sciences, Whitechapel, London, UK 4Department of Primary Care and Population Health, University College London, London, UK 5Academic Unit of Respiratory Medicine, University College London Medical School, London, UK

Correspondence to Professor Janet L Peacock, Department of Primary Care and Public Health Sciences, King's College London, 7th Floor Capital House, 42 Weston Street, London SE1 3QD, UK; janet.peacock@kcl.ac.uk

Received 10 November 2010 Accepted 24 February 2011 Published Online First 1 April 2011

ABSTRACT Objectives Time series studies have shown adverse effects of outdoor air pollution on mortality and hospital admissions in patients with chronic obstructive pulmonary disease (COPD) but panel studies have been inconsistent. This study investigates short-term effects of outdoor nitrogen dioxide, ozone, sulfur dioxide, particulate matter (PM10) and black smoke on exacerbations, respiratory symptoms and lung function in 94 patients with COPD in east London. Methods Patients were recruited from an outpatient clinic and were asked to complete daily diary cards (median follow-up 518 days) recording exacerbations, symptoms and lung function, and the amount of time spent outdoors. Outdoor air pollution exposure (lag 1 day) was obtained from local background monitoring stations. Results Symptoms but not lung function showed associations with raised pollution levels. Dyspnoea was significantly associated with PM10 (increase in odds for an IQR change in pollutant: 13% (95% CI 4% to 23%)) and this association remained after adjustment for other the pollutants measured. An IQR increase in nitrogen dioxide was associated with a 6% (0e13%) increase in the odds of a symptomatic fall in peak flow rate. The corresponding effect sizes for PM10 and black smoke were 12% (2e25%) and 7% (1e13%), respectively. Conclusion It is concluded that outdoor air pollution is associated with important adverse effects on symptoms in patients with COPD living in London.

INTRODUCTION Chronic obstructive pulmonary disease (COPD) is increasing in incidence worldwide and is currently the sixth leading cause of death.1 Patients with COPD are prone to acute deterioration in their chronic symptoms. These exacerbations of COPD were first shown to be associated with air pollutants during the London smog episode of 1952.2 There is now clear evidence that air pollution at current levels in London affects mortality3 4 and that air pollution levels in Europe lead to hospital admissions for COPD.5

Panel studies have shown adverse effects at relatively low levels of pollution. One of the earliest panel studies in patients with COPD showed that changes in pollution level were associated with exacerbations of chronic bronchitis.6 A study in Merseyside, UK involving 75 patients with COPD reported effects of ozone (O3) and sulfur dioxide (SO2) on peak expiratory flow (PEF) and respiratory symptoms recorded daily using diary

Key messages

What is the key question? < Does outdoor air pollution affect exacerbations,

respiratory symptoms and lung function in patients with COPD?

What is the bottom line? < In patients with COPD living in London, there is

evidence for adverse effects of outdoor pollution on symptoms and exacerbations, particularly for PM10, black smoke and NO2.

Why read on? < Ecological studies have shown links between

outdoor air pollution and increased COPD mortality/morbidity and this study shows similar effects in individual patients, supporting the case for causality.

cards.7 A Dutch panel study similarly reported adverse effects of PM10 (particulate matter), black smoke, sulfate and SO2 on PEF, and effects of black smoke on upper respiratory symptoms in 326 symptomatic adults.8 A panel study in Italy reported adverse effects of particles and nitrogen dioxide (NO2) on forced vital capacity (FVC) and forced expiroatory volume in 1 s (FEV1) in 29 subjects with COPD,9 and similar associations between FEV1 and particles were reported in a US COPD panel with 24 subjects.10 A New Zealand COPD panel study in 48 patients found no effect of pollution levels on PEF but observed effects of particles on night-time symptoms and nebuliser use.11 A French study conducted at a similar time to the present study analysed effects of air pollution on COPD exacerbations and reported adverse effects of O3.12

In this paper we examine the effects of a range of air pollutants on COPD exacerbations, respiratory symptoms and respiratory function, including large decrements in PEF, in a panel of 94 patients with moderate to severe COPD selected from a COPD clinic in London and followed over a 2-year period, October 1995eOctober 1997.

METHODS Subjects The East London COPD study was established in 1995 as a prospective study of the role of viral infections and environmental factors in COPD exacerbations.13e16 Subjects were patients with

Thorax 2011;66:591e596. doi:10.1136/thx.2010.155358

591

Chronic obstructive pulmonary disease

Thorax: first published as 10.1136/thx.2010.155358 on 1 April 2011. Downloaded from on January 11, 2024 by guest. Protected by copyright.

moderate to severe COPD attending an outpatient clinic at the London Chest Hospital, London. Recruitment was from October 1995 to October 1997. Inclusion criteria were: FEV1 20% below that individual's median value. These binary events were also modelled using GEEs as described above for the symptom data.

Some associations were observed for effects of single pollutants on certain symptoms and so we decided post hoc to fit selected multipollutant models to try to disentangle these effects and aid interpretation.

All effect estimates are presented in two ways: (1) representing a unit change in pollutant level (ppb or mg/m3 as appropriate) and (2) scaled to an IQR change in that pollutant level to aid interpretation. All analyses used Stata v11.

RESULTS Summary statistics for subjects and exposure data A total of 125 patients were recruited, of whom 31 were excluded for the following reasons: not continuously resident in London (13), in the study for 1.0. ORs for a symptomatic fall in PEF for a change in pollutant level equivalent to the IQR were 1.12 (95% CI 1.02 to 1.25, PM10) and 1.07 (1.01 to 1.13, black smoke). Dyspnoea was significantly associated with PM10 (OR

Table 3 Regression of respiratory function (PEF, FEV1 and FVC) on pollutant level* (previous day)

Estimatey (per unit change) (95% CI)

Estimatez (per p Value IQR change)

PEF (l/min) n?94

NO2 (ppb) O3 (ppb) SO2 (ppb) PM10 (mg/m3) Black smoke (mg/m3)

FEV1 (ml) n?28 NO2 (ppb) O3 (ppb) SO2 (ppb) PM10 (mg/m3) Black smoke (mg/m3)

FVC (ml) n?28

NO2 (ppb) O3 (ppb) SO2 (ppb) PM10 (mg/m3) Black smoke (mg/m3)

0.013 (0.002 to 0.024) ?0.015 (?0.039 to 0.009) 0.031 (?0.010 to 0.072) 0.009 (?0.006 to 0.023) 0.011 (?0.005 to 0.028)

0.005 (?0.106 to 0.116) ?0.081 (?0.258 to 0.096) ?0.035 (?0.386 to 0.315) 0.031 (?0.067 to 0.129) 0.045 (?0.113 to 0.203)

0.071 (?0.189 to 0.332) 0.162 (?0.238 to 0.562) ?0.335 (?1.192 to 0.522) 0.187 (?0.017 to 0.392) 0.166 (?0.218 to 0.551)

0.026 0.229 0.133 0.253 0.180

0.929 0.369 0.843 0.536 0.576

0.591 0.426 0.444 0.073 0.396

0.179 ?0.211

0.191 0.164 0.103

0.071 ?1.143 ?0.216

0.588 0.405

1.000 2.288 ?2.043 3.561 1.498

*In addition to individual pollutants (previous day), each model includes outdoor

temperature (average of the minimum and maximum) and season (four categories) plus

control for autocorrelation. yEstimates represent the change in lung function for a 1 unit change in pollutant level (ppb for NO2, O3, SO2; mg/m3 for PM10, black smoke). zEstimates represent the change in lung function for an IQR change in pollutant level. FEV1, forced expiratory volume in 1 s; FVC, forced vital capacity; PEF, peak expiratory flow; PM, particulate matter.

593

Chronic obstructive pulmonary disease

Thorax: first published as 10.1136/thx.2010.155358 on 1 April 2011. Downloaded from on January 11, 2024 by guest. Protected by copyright.

Table 4 Large PEF decrements, COPD exacerbations and PEF exacerbations*

Pollutant

ORy (unit change) (95% CI)

Estimatez (per p Value IQR change)

Large PEF decrements

NO2 (ppb) O3 (ppb) SO2 (ppb) PM10 (mg/m3) Black smoke (mg/m3)

COPD exacerbations

NO2 (ppb) O3 (ppb) SO2 (ppb) PM10 (mg/m3) Black smoke (mg/m3)

Symptomatic fall in PEF

NO2 (ppb) O3 (ppb) SO2 (ppb) PM10 (mg/m3) Black smoke (mg/m3)

1.000 (0.995 to 1.004) 0.996 (0.989 to 1.004) 1.001 (0.988 to 1.014) 0.999 (0.995 to 1.003) 1.001 (0.991 to 1.011)

1.002 (0.996 to 1.008) 1.005 (0.987 to 1.023) 1.002 (0.982 to 1.022) 1.004 (0.998 to 1.010) 1.003 (0.994 to 1.013)

1.004 (0.999 to 1.009) 1.002 (0.984 to 1.020) 1.004 (0.987 to 1.022) 1.006 (1.001 to 1.012) 1.007 (1.000 to 1.014)

0.844 0.362 0.890 0.712 0.851

0.469 0.598 0.878 0.234 0.497

0.137 0.840 0.622 0.029 0.050

0.994 0.950 1.006 0.985 1.009

1.032 1.070 1.010 1.075 1.029

1.058 1.026 1.026 1.124 1.066

*In addition to individual pollutants (previous day), each model includes outdoor

temperature (average of the minimum and maximum) and season (four categories) plus

control for autocorrelation. yORs are for a 1 unit change in pollutant level (ppb for NO2, O3, SO2; mg/m3 for PM10, black smoke). zORs are for an IQR change in pollutant level. COPD, chronic obstructive pulmonary disease; PEF, peak expiratory flow; PM, particulate

matter.

1.13; 95% CI 1.04 to 1.23) for a rise in PM10 across its IQR. No other symptomepollutant combinations were significant, except O3 which showed a protective association with nasal discharge/congestion (table 5).

In multipollutant models, the effect size for PM10 on symptomatic fall in PEF remained similar and borderline significant after adjustment for other pollutants (table 6). In contrast, the effects of NO2 and black smoke were weaker after controlling for PM10. For dyspnoea, the effect of PM10 was slightly stronger and remained significant after adjustment for either NO2, black smoke or both (table 6). There was no evidence of any adverse effect of NO2 or black smoke after allowing for PM10.

DISCUSSION Overall this study provided evidence for adverse effects of outdoor pollution on symptoms and exacerbations in patients with COPD living in London, particularly PM10, black smoke and NO2. Most symptoms gave ORs >1 but very few associations were statistically significant. Effect sizes were mostly larger for symptomatic fall in PEF compared with COPD exacerbations and gave significant ORs for NO2, PM10 and black smoke. Symptomatic falls in PEF events were more common than COPD exacerbations and so significance is partly due to increased statistical power. Dyspnoea was associated with higher levels of PM10 but was not significantly associated with any other pollutants. Multiple pollutant models showed that the association between PM10 and dyspnoea was stronger after adjustment for other pollutants, although this analysis was post hoc and conducted to aid interpretation of the findings. In general, symptoms are highly variable in COPD and the appearance of shortness of breath on the diary card may reflect psychological as well as mechanical effects on the airway. The occurrence of shortness of breath with a fall in PEF is suggestive of a mechanical effect on the airway by some stimulus.

Table 5 Worsening symptoms: dyspnoea, sputum purulence or sputum amount, nasal discharge/congestion, wheeze or tight chest and upper respiratory symptoms*

Pollutant

ORy (unit change) (95% CI)

Estimatez (per p Value IQR change)

Dyspnoea n?77

NO2 (ppb)

O3 (ppb)

SO2 (ppb) PM10 (mg/m3) Black smoke (mg/m3)

1.003 (0.997 to 1.008) 1.005 (0.995 to 1.016) 0.996 (0.980 to 1.013) 1.006 (1.002 to 1.011) 1.003 (0.994 to 1.012)

Sputum changes n?68

NO2 (ppb)

O3 (ppb)

SO2 (ppb) PM10 (mg/m3) Black smoke (mg/m3)

1.006 (0.999 to 1.013) 1.007 (0.992 to 1.022) 1.008 (0.988 to 1.029) 1.004 (0.997 to 1.011) 1.004 (0.992 to 1.016)

Nasal discharge or congestion n?70

NO2 (ppb)

O3 (ppb)

SO2 (ppb) PM10 (mg/m3) Black smoke (mg/m3)

0.999 (0.991 to 1.006) 0.984 (0.970 to 0.998) 1.011 (0.994 to 1.030) 1.003 (0.997 to 1.010) 1.003 (0.992 to 1.013)

Wheeze or tight chest n?70

NO2 (ppb)

O3 (ppb)

SO2 (ppb) PM10 (mg/m3) Black smoke (mg/m3)

1.002 (0.996 to 1.009) 0.992 (0.977 to 1.007) 1.002 (0.986 to 1.019) 1.004 (0.998 to 1.009) 1.002 (0.993 to 1.010)

Upper respiratory symptoms n?73

NO2 (ppb)

O3 (ppb)

SO2 (ppb) PM10 (mg/m3) Black smoke (mg/m3)

0.999 (0.990 to 1.008) 0.987 (0.969 to 1.005) 0.991 (0.971 to 1.012) 1.000 (0.993 to 1.007) 1.007 (0.990 to 1.024)

0.338 0.335 0.662 0.008 0.526

0.085 0.370 0.446 0.251 0.536

0.690 0.023 0.209 0.296 0.598

0.460 0.274 0.785 0.187 0.722

0.849 0.143 0.392 0.928 0.435

1.036 1.078 0.978 1.125 1.027

1.085 1.099 1.042 1.082 1.035

0.979 0.794 1.072 1.067 1.026

1.033 0.890 1.014 1.071 1.014

0.988 0.829 0.947 0.994 1.062

*In addition to individual pollutants (previous day), each model includes outdoor

temperature (average of the minimum and maximum) and season (four categories) plus

control for autocorrelation. yORs are for a 1 unit change in pollutant level (ppb for NO2, O3, SO2; mg/m3 for PM10, black smoke). zORs are for an IQR change in pollutant level. PM, particulate matter.

When estimated effect sizes were scaled to IQR increases in pollutant level, it was evident that estimated effect sizes were considerable: the odds of a symptomatic fall in PEF increased by 13% when PM10 increased across the IQR, and a similar size effect was observed for dyspnoea. These increases in odds represent a substantial increase in risk, if associations were real and causal, and are stronger than observed effects of raised pollution on COPD hospital admissions.5

Effects on neither mean lung function nor the binary large PEF decrements showed consistent trends, despite evidence from other panels that the binary outcome is more discriminating than mean PEF.8 24 This may reflect the high variability of PEF and/or that lung function was measured after taking medication. Importantly, the findings of adverse effects on symptoms but not mean lung function are consistent with results of ecological studies showing associations with acute events such as death, hospital admission and general practitioner consultations. They lend support to the hypothesis that effects of outdoor air pollution are greater among the very vulnerable.

Findings in this London study were consistent with those of Harr? in New Zealand11 who reported associations between particles and symptoms with similar effect sizes to ours; however, they also found no associations with lung function.

594

Thorax 2011;66:591e596. doi:10.1136/thx.2010.155358

Thorax: first published as 10.1136/thx.2010.155358 on 1 April 2011. Downloaded from on January 11, 2024 by guest. Protected by copyright.

Chronic obstructive pulmonary disease

Table 6 Further investigation of associations with PEF exacerbations and dyspnoea: single and multiple pollutant models*

Single pollutant models

Multiple pollutant models

Model*

ORy (unit change) SE

ORy p Value (unit change) SE

p Value

ORz (IQR change)

Symptomatic fall in PEF (N?78)

Model 1

NO2 PM10 Model 2

1.004 1.006

NO2 Black smoke

1.004 1.007

Model 3

PM10 Black smoke

1.006 1.007

Model 4

NO2 PM10 Black smoke

1.004 1.006 1.007

Dyspnoea n?77

Model 1

NO2 PM10 Model 2

1.003 1.006

NO2 Black smoke

1.003 1.003

Model 3

PM10 Black smoke

1.006 1.003

Model 4

NO2 PM10 Black smoke

1.003 1.006 1.003

0.003 0.003

0.137 0.029

0.003 0.004

0.137 0.050

0.003 0.004

0.029 0.050

0.003 0.003 0.004

0.137 0.029 0.050

0.999 1.007

1.002 1.005

1.006 1.000

0.999 1.007 1.001

0.003 0.002

0.338 0.008

0.003 0.005

0.338 0.526

0.002 0.005

0.008 0.526

0.003 0.002 0.005

0.338 0.008 0.526

0.997 1.008

1.001 1.003

1.008 0.996

0.998 1.008 0.998

0.003 0.003

0.709 0.042

0.004 0.005

0.654 0.306

0.004 0.005

0.083 0.953

0.004 0.004 0.006

0.725 0.064 0.907

0.983 1.140

1.025 1.049

1.126 0.998

0.980 1.137 1.006

0.003 0.003

0.380 0.007

0.004 0.006

0.760 0.598

0.003 0.006

0.007 0.455

0.004 0.003 0.007

0.578 0.005 0.733

1.017 1.031

0.961 1.159

1.156 0.961

0.970 1.168 0.979

*In addition to individual pollutants (previous day), each model includes outdoor temperature (average of the min and maximum) and

season (four categories) plus control for autocorrelation. Models 1e3 each contain two pollutants analysed together. Model 4 includes

all three pollutants. yORs are for a 1 unit change in pollution level (ppb for NO2, O3, SO2; mg/m3 for PM10, black smoke). zORs are for an IQR change in pollutant level. PEF, peak expiratory flow; PM, particulate matter.

Trenga10 reported effects of PM2.5 on FEV1 in all adults but no effects on PEF. PM2.5 data were not available when our study was conducted but since PM10 is dominated by small particles, the comparison with our study is reasonable. The adverse effects of O3 on exacerbations demonstrated in the Parisian study12 were stronger than in our study.

The estimated relationships between air pollution and symptoms and lung function in this COPD panel may have been affected by the time patients spent outdoors. Subjects recorded this for part of the study only and so, although we did adjust, full adjustment was not possible.

When this study was designed we chose to limit the use of multiple pollutant metrics to avoid overtesting. In particular we used just one measure for NO2d1 h maximumdpartly because of the belief that the peak drives health effects. However, the correlation between 1 h maximum NO2 and average daily NO2 was very high at 0.90, and so the choice would seem unlikely to matter. When our study was conducted, there was a network of black smoke monitors and so we used the monitor nearest to the patient's home to estimate their exposure. The data on the other pollutants all came from a single monitor in central London but the correlation with another monitor for PM10 was high (0.95), suggesting that this was not unreasonable. Even so, the use of multiple monitors may explain the weaker associations observed with black smoke. We modelled exposure to pollution using

previous day pollutant level as others have done, and have not looked at long lags25 which would most probably have produced stronger associations.

Daily diary data provide a powerful tool tool to investigate effects of air pollution within individuals but are resource intensive and often panels are only able to include a relatively small sample and/or a short follow-up time. The strength of this study was the relatively large sample, 94, and the lengthy 2-year follow-up period. Since compliance was very good, missing data were minimal.

Recent WHO guidelines for PM10 are 20 and 50 mg/m3 for annual and daily averages, respectively. The levels of exposure for this panel were a little higher. The WHO guidelines were largely based on ecological time series studies and cohort data on mortality. This study therefore lends support to the guideline.

In conclusion, in patients with COPD living in London, there is evidence for adverse effects of outdoor pollution on symptoms and exacerbations, particularly for PM10, black smoke and NO2. The ORs of up to 1.17 for an IQR increase in pollutant level represent substantial effects which would have important public health implications if shown to be real and causal. This deserves further investigation in larger panels.

Funding The East London COPD study was funded by the British Lung Foundation. The statistical analysis for the air pollution analyses was funded by the UK Department of Health.

Thorax 2011;66:591e596. doi:10.1136/thx.2010.155358

595

Thorax: first published as 10.1136/thx.2010.155358 on 1 April 2011. Downloaded from on January 11, 2024 by guest. Protected by copyright.

Chronic obstructive pulmonary disease

Competing interests None.

Ethics approval This study was conducted with the approval of the East London and City Health Authority Ethic Committee.

Provenance and peer review Not commissioned; externally peer reviewed.

REFERENCES

1. Murray CJ, Lopez AD. Mortality by cause for eight regions of the world: Global Burden of Disease Study. Lancet 1997;349:1269e76.

2. Logan WPD. Mortality in London fog incident. Lancet 1953;1:336e8. 3. Schwartz J, Marcus A. Mortality and air-pollution in London: a time-series analysis.

Am J Epidemiol 1990;131:185e94. 4. Anderson HR, Ponce de Leon A, Bland JM, et al. Air pollution and daily mortality in

London: 1987e92. BMJ 1996;312:665e9. 5. Anderson HR, Spix C, Medina S, et al. Air pollution and daily admissions for chronic

obstructive pulmonary disease in 6 European cities: results from the APHEA project. Eur Respir J 1997;10:1064e71. 6. Lawther PJ, Waller RE, Henderson M. Air pollution and exacerbations of bronchitis. Thorax 1970;5:525e39. 7. Higgins BG, Francis HC, Yates CJ, et al. Effects of air pollution on symptoms and peak expiratory flow measurements in subjects with obstructive airways disease. Thorax 1995;50:149e55. 8. van der Zee SC, Hoek G, Boezen MH, et al. Acute effects of air pollution on respiratory health of 50e70 yr old adults. Eur Respir J 2000;15:700e9. 9. Lagorio S, Forastiere F, Pistelli R, et al. Air pollution and lung function among susceptible adult subjects: a panel study. Environ Health 2006;5:11. 10. Trenga CA, Sullivan JH, Schildcrout JS, et al. Effect of particulate air pollution on lung function in adult and pediatric subjects in a Seattle panel study. Chest 2006;129:1614e22. 11. Harre ES, Price PD, Ayrey RB, et al. Respiratory effects of air pollution in chronic obstructive pulmonary disease: a three month prospective study. Thorax 1997;52:1040e4. 12. Desqueyroux H, Pujet JC, Prosper M, et al. Effects of air pollution on adults with chronic obstructive pulmonary disease. Arch Environ Health 2002;57:554e60.

13. Seemungal TA, Donaldson GC, Paul EA, et al. Effect of exacerbation on quality of life in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 1998;157:1418e22.

14. Seemungal TA, Donaldson GC, Bhowmik A, et al. Time course and recovery of exacerbations in patients with chronic obstructive pulmonary disease. Am J Respir Crit Care Med 2000;161:1608e13.

15. Seemungal TA, Harper-Owen R, Bhowmik A, et al. Detection of rhinovirus in induced sputum at exacerbation of chronic obstructive pulmonary disease. Eur Respir J 2000;16:677e83.

16. Bhowmik A, Seemungal TA, Sapsford RJ, et al. Relation of sputum inflammatory markers to symptoms and lung function changes in COPD exacerbations. Thorax 2000;55:114e20.

17. American Thoracic Society. Standards for the diagnosis and care of patients with chronic obstructive pulmonary-disease. Am J Respir Crit Care Med 1995;152: S77e121.

18. British Thoracic Society. Guidelines for the management of chronic obstructive pulmonary disease. Thorax 1997;52:S1e12.

19. Pitkin AD, Roberts CM, Wedzicha JA. Arterialized earlobe blood-gas analysisdan underused technique. Thorax 1994;49:364e6.

20. Anthonisen NR, Warren CPW, Nelson NA, et al. Antibiotic therapy and chronic obstructive pulmonary diseasedresponse. Ann Intern Med 1987;107:597.

21. Buck SF. A method of estimation of missing values in multivariate data suitable for use with an electronic computer. R Stat Soc (B) 1960;22:302e6.

22. Peacock JL, Symonds P, Jackson P, et al. Acute effects of winter air pollution on respiratory function in schoolchildren in southern England. Occup Environ Med 2003;60:82e9.

23. Scarlett JF, Abbott KJ, Peacock JL, et al. Acute effects of summer air pollution on respiratory function in primary school children in southern England. Thorax 1996;51:1109e14.

24. Hoek G, Dockery DW, Pope A, et al. Association between PM10 and decrements in peak expiratory flow rates in children: reanalysis of data from five panel studies.

Eur Respir J 1998;11:1307e11. 25. Stylianou M, Nicolich MJ. Cumulative effects and threshold levels in air pollution

mortality: data analysis of nine large US cities using the NMMAPS dataset. Environ Pollut 2009;157:2216e23.

Journal club

Inactivation of the N-terminal of ACE reduces bleomycin-induced lung fibrosis

This study examined bleomycin-induced lung injury in normotensive mice, termed N-KO and C-KO, which have point mutations inactivating the N- or C-terminal catalytic sites of angiotensin converting enzyme (ACE), respectively. N-KO, but not C-KO mice, exhibited a marked resistance to bleomycin-induced lung injury and fibrosis, as assessed by lung histology and hydroxyproline content (46% increase in hydroxyproline content in C-KO lungs compared with 6.9% in N-KO lungs, p ................
................

In order to avoid copyright disputes, this page is only a partial summary.

Google Online Preview   Download